Yanagisawa H, Nodera M, Kurihara N, Wada O
Department of Hygiene and Preventive Medicine, Faculty of Medicine, Saitama Medical School, Japan.
Toxicol Lett. 1998 Sep 15;98(3):181-8. doi: 10.1016/s0378-4274(98)00122-2.
A progressive fall in glomerular capillary plasma flow (QA) is observed in mercury chloride (HgCl2)-induced acute renal failure (ARF) although the site of the main lesion of this ARF is the proximal tubule. To elucidate this mechanism, we examined the expression of endothelin (ET)-1 and endothelial nitric oxide synthase (eNOS) protein at the glomerulus level in the kidneys of control rats and rats with HgCl2-induced ARF. Both ET-1 and eNOS protein were detected in the juxtaglomerular cells of afferent arterioles. The expression of ET-1 was significantly increased in ARF rats when compared to control rats. Inversely, the expression of eNOS protein was markedly reduced in ARF rats as opposed to control rats. These observations suggest the participation of the vasoconstrictor, ET-1 and the vasodilator, NO in a reduction in QA observed in HgCl2-induced ARF.
在氯化汞（HgCl2）诱导的急性肾衰竭（ARF）中，尽管该ARF的主要病变部位是近端小管，但仍观察到肾小球毛细血管血浆流量（QA）逐渐下降。为阐明这一机制，我们检测了对照组大鼠和HgCl2诱导的ARF大鼠肾脏中肾小球水平内皮素（ET）-1和内皮型一氧化氮合酶（eNOS）蛋白的表达。在入球小动脉的球旁细胞中均检测到ET-1和eNOS蛋白。与对照组大鼠相比，ARF大鼠中ET-1的表达显著增加。相反，与对照组大鼠相比，ARF大鼠中eNOS蛋白的表达明显降低。这些观察结果表明，血管收缩剂ET-1和血管舒张剂NO参与了HgCl2诱导的ARF中观察到的QA降低。
